How bad is Sevin (carbaryl) really? Below is some excellent from information gathered by the Journal of Pesticide Reform. We have highlighted items we think are of special interest. For more information on the Journal - and its publisher, Northwest Coalition for Alternatives to Pesticides (NCAP) - see <www.pesticide.org>. For the full text of these articles, go to PAN's website, <www.panna.org/panna/pestis.html>, click on Search, and enter "Sevin" into their search engine.
Carbaryl, Part 1
By Caroline Cox. Journal of Pesticide Reform, Volume 13, Number 1, Spring 1993. Northwest Coalition for Alternatives to Pesticides, Eugene, OR.
Many pesticides have gained their notoriety because of a particular human or environmental health problem. The organochlorine insecticide DDT, for example, is well known because of its ability to bioconcentrate in carnivorous animals,1 and the fumigant dibromodichloropropane (DBCP) made headlines when it caused sterility in men who worked with it.2 The insecticide carbaryl, however, is striking because its use has been associated with such a large number of health problems. From acute toxicity, suppression of immune system functions, and behavioral problems to cancer, genetic damage, and reproductive problems in both males and females, carbaryl's adverse effects span an enormous range.
Carbaryl (1-naphthyl methyl carbamate) is one of the three most commonly used insecticides in the United States with an estimated annual use of between 10 and 15 million pounds.3 ... It is a broad-spectrum insecticide and is registered for use on more than 100 different crops, animals, ornamental plants, and indoor areas.4 ... It has been registered in the U.S. since 1958.4 Previously manufactured by Union Carbide,7 the primary U.S. manufacturer is now Rhone Poulenc Agricultural Company; many of its carbaryl-containing products are marketed under the brand name Sevin.8
Mode of Action
Carbaryl is a carbamate insecticide. Like all members of this chemical family, it inhibits the action of an enzyme that is an essential component of insect, fish, bird, and mammal nervous systems. The enzyme, acetyl cholinesterase (AChE), controls the chemical reaction that transforms acetylcholine into choline after acetylcholine has been used to transmit nerve impulses across the junctions between nerves. Without functioning AChE, acetylcholine accumulates and prevents the smooth transmission of nerve impulses.9 This causes loss of normal muscle control, and ultimately death. The AChE inhibition is said to be reversible because the carbaryl disassociates from the AChE within several hours. This happens even if death has already occurred. Insecticides in the organophosphate family (malathion and diazinon, for example) also inhibit AChE, but the inhibition is not as readily reversible.10
Carbaryl can also affect a number of other enzyme systems in living things. For example, the carboxylesterases (detoxification enzymes),11 lactic dehydrogenase (enzymes that utilize sugar),12 and serine esterases (enzymes important to the function of certain immune system components)13 are all inhibited by carbaryl.
Acute and Subchronic Toxicity
Symptoms of acute carbaryl exposure in humans are malaise, muscle weakness, dizziness, sweating, headache, salivation, nausea, diarrhea, incoordination, and slurred speech. Depression of breathing ability combined with an excess of fluid in the lungs (pulmonary edema) is the usual cause of death when exposure is high.10
Carbaryl's acute oral LD50 (the dose that causes death in 50 percent of a population of test animals) in rats is 255 milligrams per kilogram (mg/kg) of body weight.5 Extrapolated to the weight of an average 70 kilogram (154 pound) human who is assumed to be as sensitive to carbaryl as are rats, this means that a dose of about 18 grams or two-thirds of an ounce would be fatal.
Lower doses of carbaryl over a longer period of time cause a variety of adverse effects. In humans, ingestion of 0.13 mg/kg/day (less than a thousandth of the LD50) caused abdominal cramps and a decrease in the ability of the kidneys to resorb amino acids.14 In rats, decreases in weight and body temperature occurred following single injections of doses of less than one-twentieth of the LD50.15 Similar doses given for two years caused kidney abnormalities in rats as well as dogs.16 In addition, drinking water contaminated with 10 parts per million (ppm) of carbaryl caused liver pathologies and reduced blood clotting activity in rats17 and single sublethal doses in rabbits reduced their heart rate and caused changes in their electrocardiograms.18
Behavioral and Neurological Effects
Given that carbaryl's primary mode of action disturbs the nervous system, it is not surprising that researchers have measured a variety of neurological and behavioral effects of carbaryl exposure. Case reports of human exposures tell some compelling stories. For example, a professor of medicine at a New England university reported that his twice daily applications of a commercial tick powder with active ingredient carbaryl to his cat had dramatic effects on the cat's personality. The pet, who had never been much of a hunter, began attacking large numbers of birds and mice. The professor's personality underwent a parallel change (in spite of the gloves and mask he wore while dusting the cat) and he was described as being in a "continual rage." Ending the tick powder treatments brought an end to the aggressive behavior in both doctor and cat within a week.19 Two other reports describe patients with a neurological condition called delayed peripheral neuropathy following carbaryl exposure. This condition, normally associated with certain organophosphates and not carbamates like carbaryl, causes nerve degeneration and paralysis of arms or legs several weeks after exposure.20 One of the patients had been exposed through ingestion of a relatively large quantity of carbaryl-containing insecticide.21 The other patient was exposed when his basement was treated for fleas with a carbaryl-containing dust.22
Carbaryl exposure has also caused behavioral and neurological problems in studies of laboratory animals. In rats, single doses of ten mg/kg (less than one-twentieth of the LD50) or less caused decreases in the responses to a battery of behavioral tests,15,23 increased tolerance for electrical shock, and decreased desire to drink water.24 Smaller doses given for two weeks slowed the speed that rats were able to run a maze and increased the number of errors that they made.25 Single sublethal injections of carbaryl reduced the success of monkeys in performing a learning task.26 In pigs, long-term (over 70 days) feeding of sublethal carbaryl doses caused incoordination of movements followed by extensive degeneration of nerves in the brain and muscles.27
Effects on the Immune System
Carbaryl's ability to decrease the effectiveness of the immune system has been documented in a variety of laboratory studies. A review of some of the immune system literature published during the 1960s and 1970s cited seven studies that found adverse effects of carbaryl in immune system function of rats and rabbits;28 a second review identified three more studies.29 The studies measured decreases in the cellular activity of the immune system, a reduction in the resistance to infection by certain diseases, a decrease in antibody development, and a decrease in the size of a part of the spleen important in immune system function. Doses were well below lethal toxic doses.
More recent studies show similar results. Rats fed carbaryl at doses as low as 1/100 of the LD50 and then infected with a bacteria had a mortality rate almost twice as high as unexposed rats.30 In goldfish cell cultures, synthesis of the immunologically important compound interferon was reduced, leading to enhanced replication of a virus.31,32 In mice cell cultures, carbaryl inhibited enzymes that were essential to proper functioning of macrophages, the cells that engulf and consume foreign bodies.33 Finally, at doses too low to cause inhibition of AChE, carbaryl exposure of human cell cultures reduced proliferation of immune system cells called large granular lymphocytes. This was caused by effects on another immunologically important compound, interleukin. These lymphocytes "contribute significantly to protection against tumor cell growth and infections,"34 so their suppression can have significant consequences. Taken together, the studies suggest striking effects of carbaryl on proper immune system function.
Effects on Reproduction
Ever since the late 1960s, when two researchers showed that female beagle dogs fed carbaryl had more stillbirths and infant deaths, decreased litter size, smaller pups, and more pups with birth defects than did unexposed mothers,35 carbaryl's reproductive hazards have been of concern.29 Adverse effects in the beagle study were found at doses approximately 1/50 of the LD50. Studies since that time have demonstrated that carbaryl can affect reproduction in a variety of species and in both sexes.
Males: Two studies at a carbaryl manufacturing facility have shown that carbaryl exposure affects the quantity and quality of sperm produced by the workers. One study found that more exposed workers had very low sperm counts than in a control group of unexposed workers.36 This result was significant based on one statistical test, but has been criticized because a second statistical test only "closely approached significance." A second study of the same sperm samples found that the number of sperm abnormalities was increased in workers who were being exposed to carbaryl while the study took place.37
Studies of laboratory animals have shown similar effects. A 1980 U.S. Environmental Protection Agency (EPA) review cited four studies (three in rats, one in another rodent) showing decreases in sperm numbers, an increase in sperm abnormalities, and a decrease in sperm mobility caused by carbaryl exposure.38 A 1986 review cited three other studies of rats with similar results.29 Some of these studies found effects at low doses. For example, 7 mg/kg per day (about 1/35 of the LD50) given over a period of nine months reduced sperm mobility and the numbers of sperm-forming cells.39
Females: Female laboratory animals of a number of species fed carbaryl suffer from reproductive problems. A 1986 review summarized 25 studies that had found reproductive problems caused by carbaryl in eight different kinds of animals. These problems included reduced fertility, increased fetal mortality, low birth weights, reduced growth and survival of babies, and birth defects.29 Some effects occur at surprisingly low doses. For example, rats fed carbaryl in doses equivalent to 1/35 of the LD50 for one year had estrous cycles significantly longer than unexposed control rats39 and pregnant monkeys given daily doses as low as 1/100 of the acute lethal dose had increased rates of spontaneous abortions.40
The most recent laboratory study of reproductive effects that NCAP has found (1991) shows a variety of reproductive hazards.41 Rats exposed to carbaryl had smaller litters, smaller babies, and more resorbed fetuses than unexposed rats. (See Figure 4.) These results were found in mice receiving a single carbaryl dose during pregnancy, as well as in those exposed for most of the pregnancy. The study also found an increased frequency of birth defects, including eye, kidney, and skeletal abnormalities, in the fetuses of carbaryl-treated mothers.
Several recent epidemiology studies have associated exposure to agricultural and household use of carbaryl with an increased risk of cancer in humans. Farmers in Minnesota and Iowa who had ever handled carbaryl had an increased risk of non-Hodgkin's lymphoma; this increased risk was statistically significant for those farmers who had handled the chemical prior to 1965 (with a risk almost four times as high as that of unexposed Minnesota and Iowa residents) or had handled carbaryl without using protective clothing (with a risk about double that of unexposed Minnesotans and Iowans).42 A similar elevated risk associated with exposure to carbamate insecticides as a group was found in a study of Nebraska farmers.43 Exposure to carbaryl used in gardens or backyard orchards in Missouri is associated with an increased risk (2.5-fold) of childhood brain cancer.44
Some of the concerns about carbaryl's carcinogenicity come from the carcinogenicity of nitrosocarbaryl, a compound that forms when carbaryl is combined with certain nitrogen-containing compounds (sodium nitrite, for example). Nitrosocarbaryl belongs to a family of compounds called N-nitrosamines of which 70 percent have been found to be carcinogenic in laboratory tests.45 Nitrosocarbaryl has been shown to form in the stomach of guinea pigs (animals whose stomachs are as acid as human stomachs) when the guinea pigs are given carbaryl and sodium nitrite.46 Nitrosocarbaryl causes skin cancers when painted on the skin of mice47 and cancers of the forestomach in rats.48,49
At least fifteen laboratory studies have been done of carbaryl's carcinogenicity.29,50,51 Three of these studies showed that carbaryl exposure caused an increase in cancer incidence: a 1970 study of rats,52 a 1982 study of carbaryl's ability to enhance lung tumor formation in mice by the carcinogen benzo[a]pyrene,51 and a 1992 study of carbaryl's ability to initiate tumors when painted on the skin of mice.50 The other studies found no relationship between carbaryl exposure and cancer incidence.
There are a number of reasons why epidemiology and laboratory studies give conflicting results. First, none of the laboratory studies meets current standards29,53 and properly done studies may show significant results. Second, all of the laboratory studies used technical grade carbaryl while humans in epidemiology studies are exposed to commercial carbaryl products which contain a variety of other ingredients in addition to carbaryl. (See "Secret 'Inert' Ingredients," below) Some of these may be carcinogenic. Third, humans are exposed to mixtures of chemicals rather than the single chemicals used in laboratory tests. Given the studies showing that carbaryl can enhance or initiate cancers caused by other compounds, it may be combinations of chemicals that are important. Finally, humans may be more sensitive to carbaryl than are laboratory animals. For example, human stomachs are more acid than rat stomachs, and therefore are more likely to promote the formation of nitrosocarbaryl.46
People are exposed to carbaryl through using the insecticide in homes and gardens, consuming residues on food, drinking contaminated water, being contaminated due to drift from nearby applications, and working with carbaryl. Detailed information about these effects will be published in the next issue of JPR (13(2); Summer 1993).
Effects on Nontarget Species
A wide variety of animals, plants, and bacteria are adversely affected by carbaryl. Not only acute toxicity, but many different kinds of chronic effects have been documented in bees, beneficial insects, fish, birds, earthworms, frogs, crop plants, nitrogen-fixing bacteria, and other species. Some effects occur at surprisingly low doses. Detailed information about these effects will be published in the next issue of JPR (Summer 1993).
The anti-ulcer drug Tagamet (cimetidine) has been shown to inhibit the breakdown of carbaryl in both laboratory animals and humans.69 This means that people exposed to both cimetidine and carbaryl will have longer and more pronounced symptoms. For example, a man who was exposed to six home treatments of a carbaryl-containing insecticide and who was also taking cimetidine suffered from headaches, memory loss, muscle weakness and cramps, anorexia, weight loss, and sleep apnea for a seven month period. Some neurological symptoms persisted for over a year.22 The acute and chronic toxicity of niridazole, a drug used to treat schistosomiasis, is also enhanced by carbaryl exposure.70
The common insecticide synergist piperonyl butoxide increases carbaryl toxicity. In fish, acute toxicity of a carbaryl-piperonyl butoxide mixture was over 100 times that of carbaryl alone.71 In addition, carbaryl increases the acute toxicity of the phenoxy herbicide 2,4-D, the insecticides rotenone (a botanical) and dieldrin (an organochlorine) as well as the wood preservative pentachlorophenol.72 Sublethal effects of the organophosphate insecticide phenthoate are also synergized by carbaryl in fish, including AChE inhibition73 and both morphological and behavioral changes.74 While the toxicity of combinations of chemicals is rarely studied, the ability of carbaryl to interact with a large number of chemical classes is striking.
One of the intermediaries used in the manufacture of carbaryl is the highly reactive compound methyl isocyanate (MIC).9 On December 3, 1984 a toxic cloud containing MIC and other reaction products escaped from a tank in a Union Carbide plant in Bhopal, India that manufactured carbaryl and aldicarb (another carbamate insecticide).75 Between 2500 and 5000 people died as a result of the accident, and up to 200,000 people were injured. Injuries included respiratory problems, eye damage, fetal and newborn deaths, suppression of the immune system, and changes in blood chemistry.76 A smaller, but similar accident occurred the following year at Union Carbide's aldicarb and carbaryl plant in Institute, West Virginia and 135 people were hospitalized.75
Secret "Inert" Ingredients
Most carbaryl-containing pesticide products contain "inert" ingredients whose identity EPA and the pesticide industry claim are trade secrets. There is little publicly available information about most of these "inerts." Some carbaryl formulations contain crystalline silica as an "inert" and others contain petroleum oils.77 EPA has listed petroleum hydrocarbons as an inert with high priority for testing because some petroleum products are suspected or known carcinogens.78
Crystalline silica causes the chronic lung disease silicosis79 and the International Agency for Research on Cancer has classified crystalline silica as having "limited evidence of carcinogenicity in humans" and "sufficient evidence of carcinogenicity" in animals.80 Silica was responsible for what has been called "America's worst industrial disaster" during the 1930s when over 700 workers died of silicosis after working on a tunneling project for Union Carbide in West Virginia.81
Other "inerts" in carbaryl formulations also pose toxicological problems. For example, exposure of prawns to sublethal concentrations of a commercial formulation of carbaryl caused more AChE inhibition than did exposure to carbaryl alone. The researchers believe that the emulsifier in the commercial formulation is responsible for the enhanced toxicity.82
Carbaryl is a neurotoxic carbamate insecticide. In humans, acute effects of carbaryl exposure include headaches, nausea, incoordination, and difficulty breathing. Carbaryl can cause a variety of behavioral effects, some of which are relatively long-term. It also suppresses several functions of the immune system. Men exposed to carbaryl have more abnormal sperm and lower sperm counts than unexposed men. In female laboratory animals, exposure to carbaryl has caused a variety of reproductive problems, including birth defects in beagle dogs and increased rate of miscarriages in monkeys. Exposure to carbaryl has been associated with a higher incidence of the cancer non-Hodgkin's lymphoma in farmers and brain cancer in children. Nitrosocarbaryl, formed when carbaryl and nitrites react, is a potent carcinogen. Both carbaryl and nitrosocarbaryl cause genetic damage in some test systems, as does carbaryl's primary breakdown product, 1-naphthol.
Carbaryl acts synergistically with a number of other insecticides and herbicides. An enormous industrial accident occurred at a carbaryl-manufacturing plant in Bhopal, India and other such plants have had significant accidents. Secret ingredients in carbaryl formulations include petroleum oils and crystalline silica, associated with the lung disease silicosis and cancer.
Carbaryl, Part 2
By Caroline Cox. Journal of Pesticide Reform, Volume 13, Number 2, Spring 1993. Northwest Coalition for Alternatives to Pesticides, Eugene, OR.
Carbaryl is one of three most commonly used insecticides in the United States.1 The first part of this article (JPR 13(1): 31-36) detailed the many toxicological problems caused by exposure to carbaryl, as well as information about its uses, mode of action, problems associated with carbaryl's synergistic interactions with other pesticides and medications, accidents at carbaryl manufacturing plants, and carbaryl formulations' "inert" ingredients. Part 2 discusses how humans are exposed to carbaryl and how carbaryl affects plants, animals, and microbes.
People are exposed to carbaryl when they consume residues on food, drink contaminated water, use the insecticide in homes and gardens, are contaminated by drift from nearby applications, or work with carbaryl.
Food residues: Carbaryl was the most commonly detected carbamate insecticide in the 1991 U.S. Food and Drug Administration pesticide residue monitoring program; it was the tenth most commonly detected pesticide. It was also one of eight pesticides detected in baby food samples.2
Carbaryl's extensive and varied uses account for the frequent occurrence of residues on food. In addition, though carbaryl is generally thought to have "short term residual properties,"3 under certain conditions it can be persistent. For example, carbaryl sprayed on bean leaves at least ten hours before rainfall was washed away slowly and "never attained 100 percent dissipation."4 Chickens treated for mites with a carbaryl dip laid eggs with carbaryl residues for 56 days after treatment.5
Contaminated water: Because of its chemical characteristics, the U.S. Environmental Protection Agency (EPA) identified carbaryl as one of the pesticides with most potential to leach into groundwater.6 It has been found in groundwater in California, Missouri, New York, Rhode Island, Virginia,7 and Wisconsin.8
According to EPA's STORET water quality database, carbaryl has been found in about 9 percent (58) of the 640 surface water samples which have been tested for carbaryl.9 Almost a fifth of the river water sampled tested in a New Jersey survey contained carbaryl10 as did summer samples from a Greek river.11
As with carbaryl residues on food crops, water can contain residues that persist much longer than would be expected. Following carbaryl spraying in a Maine forest during a simulated spruce budworm control project, residues were measured in pond water for 14 months.12 In South Carolina, residues from an experimental application of carbaryl to a sandy loam field persisted in groundwater for 8 months.13
Studies of pesticide residues in California fog have found higher than expected levels of carbaryl. Highest concentrations were found in nonagricultural areas, indicating that homeowner use of this pesticide may be an important source of fog residues.14
Household use: A recent EPA survey estimated that over 12 million (almost 16 percent) of U.S. homes used carbaryl-containing products in 1989-1990. Over 28 million applications are made annually in homes and over 31 million applications are made in yards and gardens. Only six pesticide ingredients are used more often than is carbaryl in U.S. homes.15 Carbaryl and chlorpyrifos (an organophosphate insecticide commonly used in households) were the most abundant pesticides found in a survey of house dust collected from homes in Seattle, Washington,16 and the most abundant insecticides (excluding the persistent organochlorines) in dust collected from homes in Raleigh, North Carolina.17 Carbaryl has also been found in indoor air following its application into cracks and crevices (a common treatment for household insect pests).18
Residents of homes where carbaryl is or has been used often ask about the time that carbaryl will persist in their yard, lawn, or garden. It is difficult to answer because persistence depends on weather, climate, soil type, and a host of other factors. Carbaryl's persistence in soil has been measured between two and sixteen weeks.19 Occasionally, however, it can persist much longer (up to 16 months).12,13
Drift: Humans are exposed to carbaryl when the insecticide drifts from an agricultural, forestry, or other application. Drift is an inevitable part of some application procedures. For example, a study of orchard carbaryl applications in Vermont found that aerially-applied carbaryl drifted to the most distant sampling point (about 500 yards) under all wind and atmospheric stability conditions tested.20
Drift is more extensive under conditions that favor movement of carbaryl droplets. Under "moderate" (5-7 miles per hour) wind conditions, aerially applied carbaryl drifted up to 2 miles.21 Ground applications drifted three times farther (up to 150 yards) when temperature inversions were present than when they were not.20 In a Maine spruce budworm spray program, aerially-applied carbaryl appears to have drifted 7 miles from the target area.22
Occupational Exposure: The manufacture of carbaryl and its use in agricultural or other occupational settings exposes workers to the insecticide. A 1962 study of the first U.S. manufacturing facility showed that workers had lower than normal blood acetylcholinesterase (AChE) activity and higher than normal 1-naphthol (carbaryl's major breakdown product) residues in their urine.23 Male workers have an increased frequency of sperm abnormalities and low sperm counts. (JPR 13(1):33) Agricultural workers are also exposed to this insecticide. In California (where reporting of pesticide-related illnesses has been required for longer than most other states), carbaryl was one of the top eight insecticides causing illness among agricultural workers. Most of the illnesses were associated with chronic (more than three days) exposure to carbaryl.24 Indoor uses of carbaryl also cause occupational exposure. For example, among pet handlers (workers at kennels, veterinary clinics, grooming shops, etc.) use of carbaryl-containing flea control products was associated with increased frequencies of diarrhea, coughing, difficult breathing, and congestion. These are all typical symptoms of poisoning with an AChE inhibitor.25
Special Concerns: Concern about human exposure to carbaryl is heightened by its tendency to be absorbed through skin, the failure of protective clothing to adequately prevent exposure, and potential exposure of particularly susceptible individuals.
* Skin absorbs carbaryl well. About three-quarters of the carbaryl applied to skin in experimental studies is absorbed.26 Two studies have found that skin absorbs a higher proportion of carbaryl than it absorbs a variety of other commonly used pesticides.26,27 (See Figure 3.) The skin of young rats absorbs more carbaryl than that of older rats,28 raising the possibility that children might be particularly susceptible.
* Protective clothing does not always serve its intended function. When used to protect from carbaryl exposure, it can fail because the clothing itself retains contamination from an earlier use, and because the protective barrier is permeable under certain conditions. While carbaryl is not as difficult to remove from clothing by laundering as are some pesticides, as much as 12 percent of carbaryl residues remained in clothing after a hot five minute machine laundering.29 Perspiration increases the amount of carbaryl transmitted through a variety of fabrics often used for protective clothing.30 This means that people using protective clothing in hot conditions will be exposed to more carbaryl.
* The most common disease-producing enzyme deficiency disease of humans is called glucose-6-phosphate dehydrogenase (G-6-PD) deficiency disease.31 About 13 percent of African-American males, have this inherited deficiency.32 People with a G-6-PD deficiency have a reduced life span and are sensitive to antimalaria drugs. The drugs cause a life-threatening disintegration of red blood cells in these individuals.31 Research with sheep, which are all G-6-PD deficient, indicates that carbaryl causes a similar reaction.32
Effects on Nontarget Species
Carbaryl is toxic to a wide variety of living things not considered pests, including beneficial arthropods, birds, fish, earthworms, plants, and bacteria. In almost all cases, carbaryl is both acutely toxic and causes a variety of sublethal effects.
Bees: Carbaryl is acutely toxic to bees, including the honey bee, leaf cutter bees, and alkali bees (the latter two species are important pollinators of seed alfalfa.)33 Carbaryl poisoning of beehives is an important economic problem. For example, a survey of bee poisonings in Connecticut found that carbaryl was the second most commonly detected pesticide, and that about 60 percent of contaminated hives had been poisoned with carbaryl.34
Beneficial arthropods: When carbaryl is used to kill insects and mites that cause agricultural pest problems, the predators and parasites of the pests are also killed by carbaryl. Examples can be found in a wide variety of agricultural systems, including the parasitoids of the sweet potato whitefly;35 spiders that prey on the European corn borer;36 predators of mite pests on seedless grapes,37 almonds,38 and cotton;39 parasitoids of armyworms;40 a parasitoid of the cotton bollworm;41 and aphid predators on collards.42
Effects can be dramatic. Carbaryl applied during a Japanese beetle eradication program in San Diego County, California, destroyed the parasitoids that had been introduced to control the wooly whitefly and the citrus red mite. The result was an explosion in whitefly and mite populations, causing defoliation of yard, garden, and street trees on a "massive scale."43 (See Figure 4.)
The same type of effects occur in nonagricultural ecosystems. For example, carbaryl treatment reduced the abundance of litter-decomposing insects in sagebrush, disrupting nutrient cycling;44 killed aphid predators in tallgrass prairie;45 decreased the number of pollinators, and the number of fruits set by flowering shrubs, in a forest sprayed with carbaryl to kill spruce budworm;46 decreased stonefly populations in streams sprayed with carbaryl for spruce budworm control (populations remained low for at least four years);47 and increased the survival of a disease-carrying beetle in a pine forest by killing its predators.48
Fish: Carbaryl is acutely toxic to fish. While toxicity varies depending on the species of fish tested, for four representative species concentrations of between 2 and 16 parts per million (ppm) in water cause death.49 At much lower concentrations, physiological and behavioral effects occur. For example, concentrations of less than 1 ppm cause a decrease in amino acid levels in muscles,50 damage to gill and liver cells, kidney lesions,51 and slowing of fin regeneration.52 Slightly higher concentrations cause inhibition of the synthesis of proteins in fish livers,53 decrease in the respiration rate,54 alterations of feeding and social behavior,55 and decreased growth rates.56
Reproduction of fishes is particularly susceptible to carbaryl poisoning. Concentrations of 10 parts per billion (0.01 ppm) reduced pigmentation; slowed development; and caused convulsive tremors,57 cardiovascular abnormalities, stopping of development, and vision abnormalities58 in fish embryos. Higher concentrations (10-20 ppm) reduced the number and size of eggs, increased the number of deformities and damaged the yolk.59
Carbaryl's primary breakdown product, 1-naphthol, is more toxic to a number of species of fish than is carbaryl itself. This has been demonstrated in the shiner perch, English sole, stickleback, goldfish, killifish, and several other freshwater fishes (including some of economic importance).60-62
Carbaryl bioconcentrates in fish tissues to levels between 9 and 34 times higher than those in the water in which the fish swim.63
Birds: Carbaryl is acutely toxic to birds, although the dose required to kill most species is greater than that required to kill mammals, fish or insects.64 Carbaryl also adversely affects birds at lower doses. Aerial spraying of carbaryl (to simulate a spruce budworm spray program), for example, reduced the abundance of large invertebrates in ponds. As a result, ducklings (mallard and black) living in the ponds had reduced growth rates, spent more time searching for food, and spent less time resting than ducklings on unsprayed ponds.65 A study of a spruce budworm spray program in Maine found that the carbaryl treatment reduced the numbers of tree-living arthropods and changed the feeding behavior of the warblers in the forest. Fewer warblers fed in the treated areas and they fed on lower branches.66 Another study in New Jersey found bird populations declined by about half following a gypsy moth spray program, and remained low for at least a year. The diversity and richness of species also declined.67 (See Figure 5.) Other studies have not been able to demonstrate affects on bird populations after carbaryl treatment of forests; the size of the treated area appears to be an important factor.68
In the laboratory, exposure of pigeons to carbaryl caused changes in the abundance of various kinds of blood cells. Bleeding and clotting time was "conspicuously prolonged."69
Unhatched and young birds appear to be particularly sensitive to carbaryl exposure. Injection of the insecticide into developing chicken eggs caused increased mortality,70,71 slowing of development, skeletal abnormalities,70 jaw deformities,72 and abnormal locomotion. The abnormal walking lasted for 47 days after treatment. Injection into mallard eggs caused stunted growth.73 Oral doses fed to young chicks also resulted in an abnormal gait; these alterations were visible at doses that were too low to cause measurable acetylcholinesterase (AChE) inhibition.74
Earthworms: Earthworms are sensitive to small amounts of carbaryl in soil. Concentrations as low as 1/20 of the LC50 (the concentration required to cause death of 50 percent of a population of test animals) caused inhibition of digestive enzymes,75 skin blisters,76 a decrease in weight and egg production,77 and degeneration of muscles.78 In field studies, carbaryl treatment reduced earthworm populations by between 5079 and 90 percent.80 Follow-up studies showed that populations took five80 to twelve months81 to recover and that the rate at which mineral soil was incorporated into thatch was significantly impaired during this period.80
Frogs: Sublethal concentrations of carbaryl caused more tadpoles to die during their metamorphosis into frogs while the frogs that survived were smaller. Effects were found at concentrations as low as 2 ppm, less than one-third of the acute lethal dose.82
Crustaceans: Cladoceran crustaceans (often called water fleas) are more sensitive to carbaryl than other common small pond invertebrates.83 Very low concentrations (2 parts per billion (ppb)) reduced growth, survival, and reproduction.84
Larger crustaceans are also affected by carbaryl. In addition to acute toxicity, carbaryl exposure caused changes in nitrogen and carbohydrate metabolism in prawns (edible shrimp).85,86 AChE inhibition has been measured in prawns when they are exposed to carbaryl concentrations as low as 0.1 ppb.87
Ecological impacts may be even more serious. A study of woodland ponds in northern Maine treated with carbaryl to simulate a spruce budworm control program showed that amphipod crustaceans, among the most abundant of the larger invertebrates in the ponds, were the most severely affected. Extinction of the crustaceans occurred in most of the ponds, and recolonization did not occur in some ponds by the end of the study, thirty months later.12
Crabs: Carbaryl is acutely toxic to adult crabs at concentrations between 300 and 400 ppb.88 Larval crabs are extraordinarily sensitive to carbaryl: 100 ppb causes death,89 less than 1/10 of that concentration prevents molting, and 1/1000 of the lethal concentration delays molting.90
Clams and Snails: Carbaryl is acutely toxic to snails and clams. In addition, concentrations about 1/3 of the lethal dose reduced the numbers of eggs produced by a freshwater snail91 and concentrations as low as 1/40 of a lethal concentration inhibited feeding in a marine snail.92
1-Naphthol is also toxic to clams and snails. Concentrations as low as 1 part per million (ppm) caused permanent constriction and elongation of a clams' siphons93 and concentrations as low as 2 ppm caused changes in the digestive cells of a marine snail.94
Plants: While insecticides are not usually assumed to have adverse effects on plants, carbaryl's use as a plant growth regulator (chemical thinning agent) in apples95,96 makes effects on other plants unsurprising. The following four types of effects of carbaryl have been documented in crop plants:
* Effects on reproduction. Examples include a decrease in germination success in wheat97 and decreased germination and an increase in abnormal chromosomes in vetch.98
* Effects on growth. Examples include the inhibition of seedling growth in beans,99 disrupted cell division in onion,100 distorted growth in poinsettia,35 decreased growth in peas and vetch,19 and a decrease in the weight of bolls in cotton.101
* Effects on photosynthesis. Examples include reductions in the photosynthetic rate of pecan trees102 and young soybeans.103
* Effects on nitrogen fixation. Examples include reduced colonization and spore-formation of peanut mycorrhizae,104 interference with the nitrogen-fixing mechanisms of the soil bacteria Azobacter,105 decreased photosynthesis, growth, nitrogen-fixation, and survival of a nitrogen-fixing bacteria common in rice paddies,106,107 reduced growth of the nitrogen-fixing bacteria Rhizobium,108,19 and toxicity to another nitrogen-fixing bacteria.109
Carbaryl's primary breakdown product, 1-naphthol, is as toxic as carbaryl to several nitrogen-fixing microorganisms.105,109 The combination of carbaryl and 1-naphthol is synergistically toxic to one bacteria.109
Aquatic Microorganisms: Carbaryl (and 1-naphthol) is acutely toxic to salt marsh protozoans at concentrations that might be expected in runoff from treated areas. When protozoan populations are killed, changes occur in the bacteria populations on which the protozoans feed, resulting in a "pronounced inhibition" of the ability to decompose plant material.109 In studies of pond zooplankton communities, single or repeated applications of carbaryl affected the numbers and diversity of cladocerans (water fleas), rotifers, predatory insect larvae, and phytoplankton.110-113
Humic acid (one of the kinds of dissolved organic materials found in streams) appears to synergize the acute toxicity of carbaryl to at least one aquatic bacteria. This indicates that aquatic organisms may be more susceptible to carbaryl poisoning when there is organic matter present.114
Ecosystem Effects: The importance of carbaryl's effects on nontarget organisms is probably most clearly shown by studies of how the insecticide affects an entire ecosystem.115 While such studies are rare, they can document effects that are not visible in simpler studies. A 1968 study of a carbaryl treatment of a millet agroecosystem showed that the numbers and weight of insects were reduced more than 95 percent; the reduction persisted for over 5 weeks. One result of this reduction was that litter decomposition declined because decomposer insects were killed. Spider populations were reduced for three months. While no acute effects were observed in trapped small mammals, reproduction of cotton rats was delayed by the carbaryl treatment for almost a month, allowing a competing species, the house mouse, to become dominant. Subsequent laboratory tests showed that carbaryl treatment of cotton rats causes a decrease in the number of litters and the number of live young. The study's author contrasts the short-term persistence of carbaryl with the long-term effects on insects and mammals that he found. (See Figure 6.)
Humans are exposed to carbaryl through consuming contaminated food and water, using carbaryl in homes, gardens, and offices, through drift, and through occupational exposure. Carbaryl is the tenth most commonly detected pesticide in U.S. food residues surveys. It has been found in groundwater, surface water, and fog. Almost 60 million applications of carbaryl-containing insecticides are made annually in homes and gardens. Workers in carbaryl manufacturing facilities, agricultural workers, and pet handlers are all occupationally exposed to carbaryl and have suffered adverse effects, including sperm abnormalities, AChE inhibition, diarrhea, and coughing. Carbaryl is well-absorbed by skin, particularly skin of young animals. Protective clothing can be difficult to effectively launder and transmits more carbaryl under hot, sweaty conditions.
A wide variety of nontarget animals, plants, and microorganisms are affected by carbaryl exposure. The number of sublethal effects that occur at low exposures is particularly striking. Beneficial arthropods, fish, birds, a variety of crop plants, and nitrogen-fixing microorganisms are all affected by carbaryl. Only one ecosystem study has been done with carbaryl, but it indicated that the effects on individual species result in persistent effects on ecosystems.
Northwest Coalition for Alternatives to Pesticides
P.O. Box 1393 Eugene, OR 97440
Phone: (541) 344-5044
These articles were available online through:
Pesticide Action Network North America (PANNA)
Phone: (415) 541-9140
Fax: (415) 541-9253
Carbaryl, Part 1, by Caroline Cox. Journal of Pesticide Reform, Volume 13, Number 1, Spring 1993. Northwest Coalition for Alternatives to Pesticides, Eugene, OR.
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Carbaryl, Part 2, by Caroline Cox. Journal of Pesticide Reform, Volume 13, Number 2, Spring 1993. Northwest Coalition for Alternatives to Pesticides, Eugene, OR.
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